A factor in serum which accelerates the conversion of prothrombin to thrombin; its relationship to the coagulation defect of thrombocytopenic blood.

T HE EXACT role of the platelet in blood coagulation is the subject of considerable controversy. Although thrombocytopenic plasma exhibits retarded coagulation, a prolonged clotting time is rare in thrombocytopenic purpura. ‘ This has been explained by the theory that even in severe thrombocytopenia sufficient thromboplastin is elaborated to produce normal coagulation.4 In any event, the hemorrhagic manifestations of thrombocytopenic purpura have generally been ascribed either to a great reduction in blood platelets, to capillary dysfunction5 or to inadequate clot retraction rather than to abnormalities in coagulation itself. It is the purpose of this paper to present observations which indicate that the coagulation of thrombocytopenic blood is profoundly disturbed. In a previous communication 6, 7 an agent was described in serum which accelerates the conversion of prothrombin to thrombin in the presence of thromboplastin plus calcium. While insufficient data are available to establish the identity or nonidentity of this substance with other factors reported to have similar . 9